Unit 2 Flashcards

1
Q

hernia

A

organ protrusion thru retaining str wall

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2
Q

where is there inc prevelance of hernias

A

abdm cavity

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3
Q

2 requirments needed for herniation to occur (patho)

A

weakening of supporting or retaining str

inc intra abdm pressure

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4
Q

what etiologies relate to weakening of supporting strs in herniations

A

acquired (injury, aging)

congenital (baby born w m. weakness)

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5
Q

what etiologies relate to inc abdm pressure

A

acquired (pregnancy, obesity)

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6
Q

hiatus

A

aperture opening in diaphragm for esophagus

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7
Q

what is a hiatal hernia

A

hiatus enlarges dt age(?) and inc P admn -> part of stomach enters TC

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8
Q

2 types of hiatal hernia

A

sliding

rolling

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9
Q

percent incidence in sliding hernia

A

95%

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10
Q

percent incidence in rolling hernia

A

5%

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11
Q

what happens in a sliding hiatal hernia

A

upper stomach and GEJ slide up into TC. stomach is pinched at entry point into TC

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12
Q

what percent of pts w sliding hiatal hernias are symptomatic

A

50%

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13
Q

what symptoms are present in pts w sliding hiatal hernias

A

chest pain, heart burn, reflux

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14
Q

what happens in a rolling/paraesophageal hiatal hernia

A

non upper part of stomach moves above diaphragm while GEJ remains in normal spot

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15
Q

mnfts of rolling hiatal hernia

A

chest pain
dyspnea
feeling full sooner after meals

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16
Q

why is there chest pain in a rolling hiatal hernia

A

rt anatomical repositioning of stomachq

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17
Q

why is there dyspnea in a rolling hiatal hernia

A

stomach takes up part of TC -> dec lung capacity for 02

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18
Q

why does the pt feel full sooner if they have a rolling hiatal hernia

A

dec stomach capacity AND smaller herniated pocket still fx’s normally, this mini stomach has stretch receptors so when small pocket fills -> n. sends signal of feeling full

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19
Q

tx for hiatal hernias

A

lifestyle mods
drugs for gastric reflux
sx

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20
Q

what lifestyle mods occur when txing hiatal hernias

A

avoid bending over after eating, avoid heavy meals, sleeping after meals, inc HOB to address reflux -> dec heartburn and pain

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21
Q

what drugs are used to treat gastric reflux in hiatal hernias

A

antacids
H2RA
PPI

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22
Q

what sx is used to treat hiatal hernias

A

fundoplication, reduce hernia while wrapping fundus of stomach around junction to prevent it from moving up while tightening cardiac sphincter

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23
Q

inguinal hernia

A

abdm organs protrude via inguinal ring forming hernial sac

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24
Q

what aperture do inguinal hernias exit from

A

inguinal ring

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25
Q

what is the inguinal ring

A

taught opening allowing passage of spermatic cord to exterior body

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26
Q

what is in a hernial sac

A

peritonium with organ and omentum inside

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27
Q

2 types of hernia

A

direct

indirect

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28
Q

direct hernia

A

herniation via no aperture (hiatal)

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29
Q

indirect hernia

A

herniation via present aperture (inguinal)

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30
Q

peptic ulcer disease

A

ulcerative disorder of upper GI tract (20% stomach, 80% duodenum).

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31
Q

why is there higher incidence of peptic ulcer disease in the duodenum

A

no protective lining here

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32
Q

what layers does peptic ulcer disease primarily affect

A

mucosa, deeper layers if no tx

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33
Q

how does peptic ulcer disease progress

A

with remissions and exacerbations, (acute condition that may become chronic)

34
Q

ET of of peptic ulcer disease

A

dt inf caused by heliobacter pylori

35
Q

how does heliobacter pylori colonize in the stomach

A

creates a niche and colonizes within stomach wall

36
Q

how does heliobacter pylori attatch to stomach wall

A

adhesion proteins allowing attatchment to epithelial tissue

37
Q

how does h pylori survive in acidic environment of the stomach

A

secrete Urease

38
Q

what is urease

A

enzyme that breaks down urea

39
Q

what does urease break down urea into

A

NH3 + CO2 -> carbonic acid buffer -> bicarbonate

40
Q

how does the break down of urea aid in the survival of H pylori

A

urea breaks into bicarbonate which buffers pH on a small scale allowing H pylori to live

41
Q

what does h pylori induce

A

inflm of tissue

hypergastrinemia

42
Q

hypergastrinemia

A

inc sec of gastrin hormone

43
Q

fx of gastrin

A

inc Hcl prod in host stomach.

44
Q

risk factors/offensive factors of peptic ulcer disease

A
Hcl + biliary acid
steroids & NSAIDS
chronic gastritis
smoking, alcohol, caffeine
stress
45
Q

which offensive factor is etiologic

A

Hcl and biliary acid

46
Q

what is an offensive factor

A

things that increase aggrevation of peptic ulcer disease

47
Q

which offensive factor is different then the rest? why

A

chronic gastritis

its presence makes a pt more susceptible to ulcers

48
Q

what are defensive factors

A

factors that prevent ulcer formation

49
Q

what 4 defensive factors prevent ulcer formation

A

acid regulation
intact perfusion
mucous presence
ability of mucosa to regenerate new cells

50
Q

what is to be said about the relationship between offensive and defensive factors

A

normally, defensive factors > then offensive factors

51
Q

what happens if offensive factors > defensive factors

A

makes pt more susceptible to ulcers if H pylori is present

52
Q

patho of peptic ulcer disease (2)

A

H pylori infec-> inflm mediator rls -> tissue damage

infc -> inc gastrin prod -> inc acid sec -> tissue damage dt no acid regulation

53
Q

mnfts of peptic ulcer disease

A

abdm pain
N/V
Fever

54
Q

describe mnft of abdm pain in peptic ulcer disease

A

burning and cramping dt inflm of tissue and tissue erosion by HCLl. its felt in the chest and may be described as angina pain

55
Q

why does N/V occur in peptic ulcer diesae

A

GI mnft

56
Q

when does fever occur in peptic ulcer disease

A

when H pylori is first establishing

57
Q

3 complications of peptic ulcer diseae

A

perforation of ulcer
hemorrhage
gastric obstr

58
Q

what may perforation of a peptic ulcer ->

A

peritonitis

59
Q

how does hemmorrhage of a peptic ulcer mnft?

A

occult blood in stools

60
Q

what may a gastric obstr in peptic ulcer disease be caused by

A

edema
scar tissue contraction
m. spasm

61
Q

mechanism of scar tissue contraction and gastric obstr

A

mucosa attempts to come together at points of injury pulling on the tissue around it, making area tight

62
Q

which tests are use to dx PUD

A
Hx
serology
fecal Ag
UBT
barium swallow
endoscopy
63
Q

fx of serology in PUD

A

looking for Ab’s against H pylori in blood

64
Q

fx of Fecal Ag in blood

A

testing stool for Ag’s related to H pylori / inc protein content

65
Q

what is the number one dx in PUD

A

UBT

66
Q

fx of UBT

A

pt ingests soln thats made to mark C14 if present. pt then gives breath sample 2-2.5 h later and if C14 is present h pylori is presnt

67
Q

how does UBT pick up H pylori infc

A

H pylori breaks down urea using urease, which is normally not present. If urea is being broken down into Co2 and NH3, then the C in CO2 is available to be marked by the test. the marked CO2 is then exhaled

68
Q

fx of barium swallow in PUD

A

we can do this to visualize extent of ulcerations

69
Q

fx of endoscopy in PUD

A

may be used instead of ba swallow or with it, we can image ulcers this way

70
Q

Tx for PUD

A

antacids?
triple regimen
Sx

71
Q

fx of antacids in PUD

A

for symptom relief and OTC med thats not to be used long term dt inc risk for kidney stones

72
Q

triple regimen

A

3 drugs used congruiently

73
Q

which drug categories are used in the triple regimen

A

either H2RA and 2 Abx, or PPI and 2 ABx

74
Q

how does an H2Ra work

A

block receptor for histamine binding. Normally histamine binding -> facilitates acid sec

75
Q

common H2Ra’s

A

zantac

tagamet

76
Q

how does a PPI work

A

blocks release of H+ from protein pumps -> dec of HCl prod

77
Q

what are the most common PPIs

A

Losec
Pariet
Nexium

78
Q

what is the typical 1st line tx in triple regimen

A

Losec
Amoxicillan
Nexium

79
Q

what is the typical 2nd line tx in triple regimen

A

Zantac
Amoxicillan
Biaxin

80
Q

what is the normal course of an Abx in triple regmine

A

week - 10 days

81
Q

what is the normal course of a PPI or H2Ra in triple regmin

A

weeks - months

82
Q

when is sx used to treat PUD

A

if complications arise, usually do sx repair during endoscopy